These studies are designed to study (1) the cardiac dynamic alterations occurring during the development and maintenance of various experimental hypertensions in conscious instrumented dogs and (2) to study the changes occurring in left ventricular wall tensile stress, contractility and dimensions during the development and maintenance of left ventricular hypertrophy. Dogs will be instrumented so as to permit during cardiac cycles instantaneous measurements of the changes in atrial, left ventricular and aortic pressures, left ventricular internal and external diameters and the atrial and ventricular electrograms. In some animals aortic flow will be monitored in addition. The derived variables obtained from semicontinous monitoring of these conscious instrumented dogs will be used to characterize their left ventricular functional response to forcing functions such as pacing the ventricle or graded increases in after load against which the heart will contract. After a suitable control period each of a group of instrumented animals will be subjected to a particular intervention designed to produce either experimental hypertension, left ventricular hypertrophy or both. Hypertension will be induced by either renal artery constriction, section of the aortic and carotid sinus nerves, or partial nephrectomy and salt loading. Left ventricular hypertrophy will be induced by producing either a chronic aortic constriction, bilateral arteriovenous fistula or complete heart block and experimental renal hypertension. With the aid of a dedicated small digital computer and a user interactive data acquisition and reduction system the data derived from each animal will be studied in terms designed to evaluate the three major factors, which modulate left ventricular function; preload changes, afterload changes and changes in myocardial contractility. An effort will be made (1) to evaluate the nature and significance of a "cardiac factor" in the pathogenesis of experimental hypertensions and (2) the significance of wall tensile stress changes in the development and maintenance of left ventricular hypertrophy.